MHD- Lec #3 - Ischemic Heart Disease Flashcards
State the myocardial infarction morphology during the following time frame:
- 30 min - 4 hours
- 4 - 12 hours
- 12- 24 hours
- No gross or light microscopic changes
- Beginning coagulation necrosis
- loss of nuclei (pyknosis) - Gross - Dark mottling (hyperemic myocardium)
Ongoing coagulation necrosis
Pyknosis of nuclei
State the myocardial infarction morphology during the following time frame:
- 1 - 3 days
- 3 - 7 days
- 7 - 10 days
- Gross – mottled (red/yellow)
Loss of nuclei and myocytes
Neutrophil infiltrate - Myocyte disintegration, phagocytosis of dead cells (increased neutrophil infiltrate)
YELLOW!
3.
Well-developed phagocytosis (macrophages) and early granulation tissue
State the myocardial infarction morphology during the following time frame:
10 -14 days
2 - 8 weeks
Granulation tissue - neovascularization
2 - 8 weeks
Scar formation
What are 3 laboratory tests for MI? Which is best?
- Troponin I (most specific & sensitive)
- CK
- Myoglobin (low sensitivity)
Describe stable & vulnerable plaques
Vulnerable plaques: Lipid rich atheromas Thin fibrous caps Inflammation Moderately stenotic - 50-75%
Stable plaque
- thick fibrous cap with mature dense collagen
2 - Unstable Angina Pectoris
Atherosclerotic plaque disruption Thrombogenic plaque components, subendothelial basement membrane exposed Platelets activation, aggregation Vasospasm Partially occluding thrombus
Stable (Typical) Angina Pectoris
Chronic stenosing coronary atherosclerosis (>75% reduction of lumen area)
Increased cardiac demand and workload needs unmet
Substernal chest pressure (ischemic myocytes = chest pain)
Physical activity, emotional excitement
Relieved with rest (decreased myocardial demand)
Vasodilator, nitroglycerin
What are the signs and symptoms of left heart failure?
Right?
Left:
Paroxysmal Nocturnal dyspnea
Orthopnea
Pulmonary Edema
Right: Heptomegaly JVD Peripheral Edema Ascites
Describe diastolic & systolic HF
Systolic Deterioration of myocardial contraction decreased EF* (60-70% is normal) below 40% for systolic myocytes are unable to generate enough contractile force
Diastolic
Inability of heart chamber to relax, expand, and adequately fill during diastole
3- Prinzmetal Variant Angina
Coronary artery spasm
Unrelated to physical activity, heart rate, blood pressure
Responds to vasodilators
TRANSMURAL and thus results in ST elevation (like an MI)
- but markers will not be present
Occlusive thrombus formation results in what?
MI
What is LDH and how does it change in an infarcted myocardium?
Triphenyltetrozolium chloride stain (LDH substrate)
Infarcted myocardium does not stain due to enzyme depletion (leakage
What are the consequences of reperfusion injury? (3)
Reperfusion INJURY = Restoration of blood flow leads to local myocardial damage
Free radical production
- Myocyte hypercontracture, increased Ca
- Leukocyte aggregation proteases, elastases
- Mitochondrial dysfunction apoptosis
Subendocardial transmural infarcts are often a result of what?
How does the infarct usually appear when the cause is global hypotension? (circumferential or transient/partial)
diffuse stenosing coronary artherosclerosis & reduction in coronary flow
- rarely evidence of plaque disruption or superimposed thrombus (thrombus may have been lysed prior to myocardial necrosis)
may result from prolonged and severe decrease in BP = SHOCK
- hypotension results in CIRCUMFERENTIAL infarct